Antidepressive Effect of Mirtazapine in Post-Myocardial Infarction Depression Is Associated with Soluble TNF-R1 Increase: Data from the MIND-IT

Background: Depressive disorder after myocardial infarction (MI) is associated with increased cardiac morbidity and mortality. Immune activity such as inflammation might be implicated as an underlying mechanism. The purpose of this study is to investigate whether the response to an antidepressant in post-MI depression is associated with changes of inflammatory markers in serum. Methods: In a double-blind placebo-controlled study with mirtazapine 30 mg/day (50 patients), the antidepressive effect was related to immune activation parameters. The cytokines interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha), the soluble cytokine receptors sIL-6R, sTNF-R1 and sTNF-R2, and the inflammation-sensitive plasma proteins C-reactive protein and neopterin were assessed. Results: Subgroup analyses revealed a highly significant correlation of pronounced sTNF-R1 increase with a decrease in depressive symptoms in antidepressant responders. Conclusion: Significant effects on inflammation accompany the therapeutic efficacy of mirtazapine in contrast to the therapeutic efficacy of placebo and the nontherapeutic efficacy of mirtazapine.